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Coronary heart disease in African Americans:

primary and secondary prevention L U T H E R T. C L A R K , MD, A N D O B I N N A Y A EMEROLE, M D

Coronary heart disease develops sooner in African Americans than in whites and causes a higher rate of mortal-ity. Because multiple risk factors and risk factor clustering are common, efforts at primary and secondary prevention in this population need to address the total risk-factor profile.

MiM-.VUiM Cigarette smoking, hypertension, diabetes mellitus, obesity, left ventricular hypertrophy, and physical inactivity are all more prevalent in blacks than in whites. Further, ac-cording to the National Health and Nutrition Examination Survey, blacks are 1.5 times more likely to have multiple risk factors than their white counterparts. Diet, weight reduc-tion and control, increased physical activity, smoking cessa-tion, and other nonpharmacologic measures are the cornerstones of therapy and should receive special emphasis.

When pharmacologic therapy is required, selection of the drug to use requires consideration of benefits, concomitant dis-eases, costs, and effects of treatment on quality of life.

AMERICANS OF WEST African ancestry are at increased risk for car-diovascular disease

mortality. Much of the higher risk is due to higher prevalences in Af-rican Americans of factors that can be modified.

Treating multiple, concomitant risk factors can be challenging, and formal practice guidelines have yet to be developed. But to be effec-tive, primary and secondary pre-vention strategies will have to ad-dress the total risk-factor profile. This paper reviews how physicians and other health care providers can improve the cardiovascular health of their black patients. INDEX TERMS: CORONARY DISEASE; RISK FACTORS; AFRICAN AMERICANS

CLEVE CLIN J MED 1995; 62:285-292

From the Division of Cardiology, Department of Medicine, State Univer-sity of New York Health Science Center, Brooklyn.

Address reprint requests to L.T.C., Division of Cardiology, Department of Medicine, State University of New York Health Science Center, 450 Clark-son Avenue, Box 1199, Brooklyn, NY 11203.

B A C K G R O U N D

Coronary heart disease (CHD) is the leading cause of death for African Americans.1,2 CHD preva-lence rates are similar in black men and white men, but higher in black women than in white women.3"5 On average, CHD de-velops about 5 years earlier and has a higher associated mortality rate among blacks than among whites of the same age, at least through age 64 for men and age 74 for women.4,5 In addition, although the age-adjusted CHD death rate

SEPTEMBER • OCTOBER 1995 CLEVELAND CLINIC JOURNAL OF MEDICINE 2 8 5

C O R O N A R Y H E A R T D I S E A S E • C L A R K A N D E M E R O L E

in the United States has been declining, it is declin-ing less for African Americans than for whites.6

The reasons for the racial disparities in CHD morbidity and mortality have not been elucidated. Blacks have a higher prevalence of risk factors than whites, and this may contribute to differences in disease manifestation and natural history. The pre-dictive value of conventional risk factors for the presence and severity of CHD appears to be similar in blacks and whites.7 However, the prevalence of CHD is similar in black and white men, even though black men have a greater risk-factor burden; higher levels of high-density lipoprotein (HDL) in black men may account for this paradox.8"10

D Y S L I P I D E M I A IN A F R I C A N A M E R I C A N S

Studies have generally found African Americans to have similar or lower total cholesterol, low-den-sity lipoprotein (LDL), and very-low-density lipo-protein (VLDL) levels compared with whites, but higher HDL levels, especially in men.8,9,11 The Na-tional Health and Nutrition Examination Survey III (NHANES III) found the age-adjusted mean total cholesterol level to be 201 mg/dL in black men and 205 mg/dL in white men, black women, and white women.12

There are limited data on the importance of cho-lesterol as a risk factor in African Americans. How-ever, among those screened for the Multiple Risk Factor Intervention Trial, the relationship between serum cholesterol level and CHD mortality was vir-tually identical in African American and white men over an average follow-up of about 12 years.12

Lipoprotein (a) Lipoprotein (a), or Lp(a), consists of an LDL

molecule covalently linked by disulfide bonds with apoprotein (a).13 Apoprotein (a) resembles the fi-brinolytic enzyme plasminogen, with a 94% amino acid homology. It has been postulated that Lp(a) may have a prothrombotic effect by competitively binding to plasminogen receptors and inhibiting the thrombolytic activity of tissue plasminogen ac-tivator.

Several investigators have reported correlations between elevated levels of Lp(a) and CHD,14"16 and higher Lp(a) levels in blacks than in whites.17"19 In a longitudinal study, 50% of black physicians had ele-vated Lp(a) levels, compared with only 17% of white physicians.20

N O N L I P I D C H D R I S K F A C T O R S IN A F R I C A N A M E R I C A N S

Hypertension and left ventricular hypertrophy

Both systolic and diastolic hypertension are asso-ciated with increased rates of cardiovascular disease. Hypertension is more prevalent in blacks than in whites, develops at a younger age, and is associated with rates of morbidity and mortality three to five times higher. The principal structural alteration of the heart in patients with hypertension is left ven-tricular hypertrophy (LVH)—a relatively uniform increase in left ventricular thickness with little change in ventricular volume.21 The prevalence of LVH by echocardiography in patients with mild to moderate hypertension is 43% to 48%.21 Although much of the mortality and morbidity of hyperten-sion appears to be related to LVH, the predictive value of LVH for morbidity and mortality is inde-pendent of hypertension and other atherosclerotic cardiovascular risk factors.22 Arrhythmias are more frequent and severe in LVH, and when myocardial infarction occurs in patients with LVH, it is apt to be more extensive.22 Hypertension and hypertensive heart disease appear to provide a substrate upon which CHD develops in blacks that is different compared with whites, and this may contribute to the increased morbidity and mortality in those pa-tients who do develop CHD.

Diabetes mellitus Both non-insulin-dependent diabetes mellitus

(NIDDM) and insulin-dependent diabetes mellitus (IDDM) are serious health problems in the United States, affecting more than 13 million Americans. NIDDM is far more common, with prevalence rates disproportionately higher in African Americans than in whites.22 Both NIDDM and IDDM increase the risk for CHD about threefold in men and even more in women. Although some of this increased risk appears to be related to alterations in serum lipoproteins, the diabetic state itself increases risk independently of its effects on the lipid profile.

The mechanisms responsible for the excess diabe-tes and cardiovascular risk in African Americans may be related in part to insulin resistance,23 al-though a recent study by Banerji and colleagues24

suggests distinct clusters of diabetic African Ameri-cans have clinical insulin resistance, whereas others are insulin-sensitive.

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Cigarette smoking Cigarette smoking is a strong risk factor for CHD,

peripheral vascular disease, and other atheroscle-rotic diseases. The overall prevalence of cigarette smoking is higher among black men than white men, although black men smoke fewer cigarettes per day.25 Data among women are conflicting, with some studies suggesting greater prevalence among black women than white women and other studies finding no differences.26"28

Obesity Total body obesity. Obesity is associated with in-

creased risk for CHD in men and women. The in-creased risk appears to be mediated chiefly through the metabolic consequences of obesity (glucose in-tolerance, diabetes mellitus, hypertension, de-creased HDL, and increased LDL and VLDL); the contribution of obesity independent of these associ-ated conditions is controversial.

Abdominal obesity. Although the relation of obe-sity per se to CHD risk is controversial, when obesity is predominantly abdominal (upper body, abdominal, central, visceral, android, apple-shaped) rather than gluteofemoral (lower body, gynecoid, pear-shaped), the risk for systemic hypertension, hyperinsulinemia, diabetes mellitus, lipid abnormalities, and CHD is increased.29-33 These findings may be especially im-portant in black women, in whom obesity occurs twice as frequently34 and in whom abdominal obesity is more common35 than in white women. Available data indicate that the risk is increased when the waist-to-hip ratio exceeds 0.90 for men and 0.80 for middle-aged and elderly women.2943,36

Physical inactivity Regular physical activity of moderate intensity

provides an element of protection against CHD.37

The protection appears to be partly related to a direct effect on the heart and arteries and partly a result of favorable effects on HDL, blood pressure, body weight, and insulin resistance. Blacks partici-pate less often in regular physical activity than do whites, independent of income and education.38

R I S K F A C T O R C L U S T E R I N G

CHD risk factors often occur in combination or clusters,39,40 conferring a synergistic effect. In adults age 25 to 74 examined in NHANESII, 59% of black women, 53% of white women, 71% of black men,

and 63% of white men had at least one cardiovascu-lar risk factor.41 In this same study, black subjects were 1.5 times more likely to have multiple risk factors than were their white counterparts.

Since cigarette smoking, hypertension, diabetes mellitus, obesity, LVH, and physical inactivity are all more prevalent in blacks than in whites, one would expect blacks to have multiple risk factors more often. Forty percent of Americans with hyper-tension have high blood cholesterol; 46% of those with hypercholesterolemia have hypertension; and hypertension, hypertriglyceridemia, and diabetes mellitus are two to three times more common in obese than in nonobese people. Dyslipidemia has proved to be a major component among clustered risk factors, especially in the presence of diabetes.

Some clusters of CHD risk factors have been de-fined as syndromes. Reaven42 has termed the cluster of hypertension, hyperinsulinemia, glucose intoler-ance, hypertriglyceridemia, elevated levels of VLDL and intermediate-density lipoprotein (IDL), and low levels of HDL as "Syndrome X"; Williams43 has termed a similar cluster "dyslipidemic hyperten-sion." Kaplan44 refers to the combination of abdomi-nal obesity, hypertension, diabetes mellitus, and lipid abnormalities as the "deadly quartet."

Why risk factors cluster in some patients is un-known. Both genetic and environmental factors have been implicated. Insulin resistance and hyper-insulinemia appear to be pivotal to clustering and to contribute to the pathogenesis of the coexistent hy-pertension, diabetes, dyslipidemia, and atheroscle-rosis. Most of the studies reporting a relationship between insulin concentrations, blood pressure, and risk factor clustering have been conducted in white populations. Investigations in blacks and Hispanics have produced conflicting results, with some studies supporting an association between hyperin-sulinemia and blood pressure45,46 and others not.47,48

Relatively little information has been generated about the specific role of risk factor clustering and CHD risk in African Americans, and effective strategies and interventions that might reduce such clustering are lacking.

I M P L I C A T I O N S FOR T H E R A P Y

The high CHD morbidity and mortality rates in African Americans can, to a large degree, be ac-counted for by the high prevalence of CHD risk factors in this group. Many of these (cigarette smok-



TABLE 1 FACTORS THAT INFLUENCE THE DECISION TO INITIATE CHOLESTEROL-LOWERING THERAPY*

Risk factors Age

Men > 45 years Women > 55 years or premature menopause

without estrogen replacement Family history of premature coronary heart disease* Current cigarette smoking Hypertension Low high-density cholesterol (HDL) level (< 35 mg/dL) Diabetes mellitus

Protective factor High HDL cholesterol level (> 60 mg/dL)

*Adapted from the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, reference 49 Myocardial infarction or sudden cardiac death before age 55 in father or other male first-degree relative, or before age 65 in mother or other female first-degree relative

ing, hypertension, physical inactivity, and obesity) are modifiable and thus present opportunities for primary and secondary prevention.

Diet and physical activity All modifiable risk factors should be approached

vigorously in patients with hypercholesterolemia. Patients who smoke cigarettes should be urged to stop. Dietary modification is the cornerstone of therapy for patients with hypercholesterolemia, hy-pertension, obesity, or diabetes mellitus. The princi-ples of dietary modification for each of these disor-ders are similar and include reducing the intake of calories, saturated fat, total fat, cholesterol, and al-cohol. Weight reduction and control and increased physical activity are also essential for effective man-agement. Even limited weight loss is often helpful. It is important to remind patients that weight reduc-tion and control are long-term rather than short-term therapies, and success will be achieved only through long-term lifestyle modifications that em-phasize both nutritional balance and physical activ-ity. Moderate exercise helps in losing weight, lower-ing cholesterol, reducing hyperinsulinemia (even without weight loss), lowering blood pressure, im-proving cardiovascular fitness, and decreasing over-all cardiovascular risk.37

Treating hypercholesterolemia T h e National Cholesterol Education Program's

Adult Treatment Panel (ATP) recently released re-vised and updated recommendations for treating adults with hypercholesterolemia.49 In specific refer-ence to African Americans, the ATP noted that although LDL levels are similar in blacks and whites (and HDL levels are higher in blacks), efforts to reduce cholesterol and other C H D risk factors in African Americans are especially important because of their higher C H D mortality rates at younger ages and their higher prevalence and severity of hyper-tension, diabetes mellitus, cigarette smoking, and physical inactivity.

The ATP report addressed several new issues that have special significance for treating African Ameri-cans with high blood cholesterol. These included:

C H D risk status as a guide to intensity of therapy. The intensity of treatment of hypercholesterolemia should depend on the individual patient's risk status. Patients should be placed into one of three risk categories in order to determine the most appropri-ate cholesterol-lowering therapy: (1) those at high-est risk because of previously diagnosed C H D or other atherosclerotic disease (peripheral arterial dis-ease or symptomatic carotid artery disease); (2) pa-tients without evident C H D but who have multiple other C H D risk factors and thus are at high risk; and (3) patients with hypercholesterolemia but who are otherwise at low risk.

Primary prevention. Primary prevention refers to the treatment of high blood cholesterol in patients without evident CHD. Patients with high-risk LDL levels (> 160 mg/dL) and those with borderline high-risk levels (130 to 159 mg/dL) who have two or more risk factors (Tables 1 and 2) should be evalu-ated clinically and receive active cholesterol-lower-ing dietary therapy. Table 2 summarizes the choles-terol levels at which to initiate dietary therapy and consider drug treatment in patients with and with-out CHD.

Secondary prevention. Treatment of elevated LDL in patients known to have C H D or other atherosclerotic disease is referred to as "secondary prevention." These patients should begin dietary treatment if their LDL concentrations exceed 100 mg/dL. The goal of therapy is to reduce the LDL concentration to 100 mg/dL or less.

Drug therapy. In secondary prevention, drug ther-apy is generally indicated if the LDL level equals or exceeds 130 mg/dL despite a trial of maximal dietary therapy. If the LDL level remains in the range of 100 to 129 mg/dL, the potential benefits of drug therapy



must be weighed against possible side effects and costs. For primary pre-vention, drug treatment can be considered for adults whose LDL levels equal or exceed 190 mg/dL with fewer than two other risk factors or 160 mg/dL with two or more other risk factors. In young men (35 years or younger) and pre-menopausal women who are otherwise at low risk, drug therapy should be reserved for those with LDL levels of 220 mg/dL or higher.

T h e major drugs for cholesterol lowering are the bile-acid sequestrants (cholestyramine and coles-tipol), nicotinic acid, and the 3-hydroxy-3-methyl-glutaryl-coenzyme A ( H M G C o A ) reductase in-hibitors (ie, the "statins"—lovastatin, pravastatin, simvastatin, and fluvastatin). T h e fibric acid deriva-tives (gemfibrozil, clofibrate) and probucol are not listed as major drugs because they do not usually produce substantial reductions in LDL. The bile-acid sequestrants are useful in patients with moder-ately elevated LDL, especially young adult men and premenopausal women, because they do not cause systemic toxicity. Nicotinic acid lowers total choles-terol and triglyceride levels and raises HDL levels, but has several side effects that may limit its use. The statins appear relatively safe and are very useful for treating severe forms of hypercholesterolemia and for lowering the LDL level maximally in secon-dary prevention.

Estrogens may be useful as specific therapy for lipid modification in some postmenopausal women. Find-ings from observational10 and prospective studies" sug-gest that estrogen replacement therapy has a beneficial effect on lipid levels and reduces C H D risk in post-menopausal women. Therefore, patients who require estrogens for other indications (ie, osteoporosis), may derive additional benefit in terms of lipid modification and overall cardiac risk reduction.

A P P R O A C H TO M U L T I P L E R I S K F A C T O R S

T h e management of high blood cholesterol in African Americans is complicated by the frequent coexistence of other risk factors such as hyperten-sion, diabetes, and obesity. W h e n approaching a

T A B L E 2 TREATMENT DECISIONS BASED ON LOW-DENSITY LIPOPROTEIN LEVELS*

Risk g r o u p

Low-density l ipoprotein level (mg/dL)

Risk g r o u p Threshold for diet therapy

Threshold for d r u g therapy

Goal of therapy

With coronary heart disease (CHD) > 100 > 130 < 100 Without CHD and two or more risk factors > 130 > 160 < 130 Without CHD and with fewer > 160 > 190 < 160

than two risk factors

Adapted from the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, reference 49

patient with high blood cholesterol, the potential impact of treatment for these other conditions must be kept in mind.

Hypercholesterolemia and c o n c o m i t a n t hypertension

High blood cholcstcrol and hypertension fre-quently coexist in African Americans. Patients with high blood cholesterol have a higher-than-expected prevalence of hypertension, and patients with hy-pertension have a higher-than-expected prevalence of high blood cholesterol. Diet, exercise, and other nonpharmacologic therapies are the essential first step for both hypertension and hyper-cholesterolemia. Emphasis should be placed on weight reduction in overweight patients, as well as on decreasing the intake of saturated fat, total fat, cholesterol, and alcohol.

W h e n drug therapy is required to lower the blood pressure, one should consider the treatment's ex-pected benefits, its effects on quality of life, con-comitant diseases, and the cost of treatment. Prefer-ence should be given to antihypertensive agents that do not adversely affect lipid levels. Calcium antagonists, angiotensin-converting enzyme inhibi-tors, hydralazine, minoxidil, potassium-sparing diu-retics, and reserpine have minimal if any effects on lipid levels. Thiazide diuretics can cause modest and often transient increases (5 to 10 mg/dL) in the serum levels of total choles tero l , LDL, and triglycerides but have little or no adverse effects on HDL. The effects of loop diuretics are similar to those of thiazides, with increases in total and LDL cholesterol, whereas HDL levels are generally lower in patients receiving furosemide. Beta blockers without intrinsic sympathomimetic activity ( I S A ) or alpha-blocking properties tend to reduce HDL, increase triglycerides, and have variable effects on



total serum cholesterol. Beta blockers with ISA and the beta blocker labetalol (which has alpha-1-ad-renergic blocking properties) produce no apprecia-ble changes in lipid levels. Although the effects of antihypertensive drugs on the efficacy of lipid-low-ering agents have not been carefully evaluated, among participants in the Coronary Primary Pre-vention Trial taking thiazide diuretics, LDL levels did not decrease as much as in those not using thiazide diuretics.48

Thiazide diuretics have proven particularly valu-able for treating hypertension in African Ameri-cans. Therefore, even though thiazides may ad-versely affect lipids in some patients, their use should not be avoided if they are needed to achieve optimal blood pressure control. Their possible ad-verse effects on lipids should be balanced by consid-erations of efficacy, safety, and tolerability.

In selecting lipid-lowering therapy, several po-tential adverse effects on blood pressure control should be kept in mind. Bile-acid sequestrants may decrease the absorption of thiazide diuretics and propranolol, and these antihypertensive medica-tions should therefore be given 1 hour before or 4 hours after the sequestrant. Nicotinic acid may en-hance the decrease in blood pressure caused by vaso-dilators. Fibric acid derivatives are more likely to produce myopathy in patients with renal failure, and thus the dosage should be decreased in these pa-tients, who should be carefully monitored.

Diabetes and dyslipidemia In dyslipidemia secondary to untreated or poorly

controlled diabetes, triglyceride levels are high, HDL levels are low, and LDL levels tend to be in the normal range or mildly elevated. In managing dia-betic patients, attention must be given to reversible risk factors, especially cigarette smoking and weight control. Control of hyperglycemia will also help to lower cholesterol and triglyceride levels. The treat-ment of coexisting hypertension should be under-taken with lipid-neutral antihypertensive agents. Adherence to a diet low in saturated fat and choles-terol may further correct the dyslipidemia.

Some clinicians view diabetes as a special case and suggest that diabetic patients undergo aggres-sive lipid-lowering therapy, similar to that given patients with established CHD, especially patients who have other risk factors. This is true for women as well as men, since the protection against CHD enjoyed by women appears to be lost in the pres-

ence of diabetes. Diabetic patients who need to reduce their LDL levels markedly often require drug therapy. Bile acid sequestrants are effective but may raise triglyceride levels (which may already be high in diabetic patients). Nicotinic acid is relatively contraindicated in patients with NIDDM since it tends to worsen glucose tolerance. Fibric acid de-rivatives effectively lower triglyceride levels and may be preferred when hypertriglyceridemia pre-dominates. The statins are generally the most prac-tical agents to use in diabetic patients with hyper-cholesterolemia and have the advantage of producing a marked reduction of LDL levels with a moderate decrease in triglycerides, but they in-crease HDL levels only modestly.

C O M P L I A N C E C O N S I D E R A T I O N S

Although the benefits of lowering the choles-terol level and blood pressure, stopping smoking, and exercising are well documented, many patients do not adhere to recommended therapy and thus do not succeed in lowering their risk. Approximately 50% of patients with hypertension fail to keep fol-low-up appointments, and only 60% take medica-tions as prescribed. From 15% to 46% of patients taking lipid-lowering drugs discontinue them within the first year, depending on the specific agent prescribed.52 The reasons for poor adherence with recommended therapy are multiple and in-clude poor doctor-patient communication, cost of therapy, and side effects of medications. Physicians and patients must be mutually committed to the goals of therapy and to achieving control of risk factors.

Physicians must select therapy that is conven-ient, affordable, and effective and that minimally detracts from quality of life. They must give clear instructions to their patients, spend time educating them about the importance of controlling risk fac-tors, and communicate in a positive manner (giving reassurance, support, and encouragement) rather than a negative manner (showing anger or anxiety). Physicians must also regularly monitor patient ad-herence and drug side effects. Failure to monitor patients effectively long-term contributes to non-compliance, as shown by the numbers of hyperten-sive patients lost to medical follow-up or who con-tinue in medical care but miss appointments and fail to follow physician advice.

Patients, on their part, must keep follow-up ap-



pointments, follow nonpharmacologic recommen-dations, and inform their physicians and nurses about other medications they may be taking and about problems with medications.

S U M M A R Y A N D C O N C L U S I O N S

The myth that African Americans are immune to CHD has been largely dispelled. African Americans have a high level of CHD risk factors and are at increased risk of CHD mortality. Risk factor modifi-cation for both primary and secondary prevention is therefore especially important. Diet, weight reduc-tion and control, increased physical activity, and other nonpharmacologic measures are the corner-stones of therapy and should receive special empha-

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